British researchers have discovered a link between human obesity and a mutation of a specific gene associated with hunger. Their observations could also point to a new approach to treat type 2 diabetes.

According to Medical News Today, University of Cambridge researchers have determined that a mutation associated with a gene known as KSR2 could be responsible for the hunger pangs described by many obese patients. It could also be responsible for slowing their metabolism so that they burn calories less efficiently than other individuals.

Prior studies showed that when researchers deleted the KSR2 gene in mice, the rodents became obese. The goal of the UK researchers was to determine if the same thing happened in human beings. They published the findings of the study of 2,101 children with early-onset obesity in the journal Cell. The results suggest that blaming childhood obesity on insufficient physical activity, overeating in general, and failure to adhere to U.S. Department of Agriculture school meal standards might represent only the tip of the iceberg.

The incidence of obese U.S. youngsters between 6 and 11 years old has jumped from 7 percent in 1980 to almost 18 percent in 2010, the Centers for Disease Control and Prevention reports. Among adolescents, the rate skyrocketed from 5 to 18 percent. In 2010, more than 1 of every 3 children and adolescents were either obese or overweight.

When the British team compared the genetic sequences of the obese youngsters with those of children at a healthy weight, they made a startling discovery. The subjects who showed a mutation in KSR2 also showed signs of a heightened appetite, slower metabolism, slower heart rate, and severe insulin resistance when compared to those who had a normal gene. Additional work showed that KSR2 mutations interfered with metabolic processes, like oxidation of glucose and fatty acids.

These outcomes demonstrated that genes can have a role in the development of obesity by reducing the body’s metabolic rate. An affected individual cannot burn calories as efficiently as someone without the mutation.

Using metformin, a diabetes medication, the scientists discovered they could increase low fatty-acid oxidation in cells where mutations of KSR2 were present. Their findings suggest the possibility of an innovative type of treatment based on regulating the protein encoded by KSR2. Using a pharmacological approach to regulate activity of this gene could eventually become a new therapy for type 2 diabetes and obesity. At its simplest level, the study suggests why some individuals gain weight more easily than others do.

Vonda J. Sines has published thousands of print and online health and medical articles. She specializes in diseases and other conditions that affect the quality of life.